| Cerebral amyloid angiopathy(CAA) is also called as cerebral congophilic angiopathy or cerebrovascular amyloidosis, and the term 'CAA' is widely used now. Its definition is the amorphous, and intensely hyaline eosinophilic material invading cerebral microvessels including small and medium-sized arteries(arterioles),venules and capillary vessels and CAA gives a characteristical staining appearance by light microscopy. With the effective control of risk factors of cerebral vascular diseases and the rapid ageing of the public population, the incidence of stroke caused by arteriosclerosis and hypertension is getting falling. Thus the clinical significance of CAA-related cerebral hemorrhage(and possible cerebral infarctions) is gradually recognized. Up to now, there are few domestic papers concerning on the clinical and pathological study on CAA-related cerebral hemorrhage. The present study is consisited of the clinical and neuropathological data of five patients with CAA-related cerebral hemorrhage and is divided into three parts. The clinical autopsy data was obtained from the Department of Neurology, Shenyang General Hospital of PLA during 1983 to 1985.In the five cases studied,there were four males and a female, they were chosen from 101 total autopsied brains which were screened by HE and Congo red staining and aged from 54 to 71years old, their mean age was 65.6(7.1 years old.Part one is focused on clinical material. There was history of moderated hypertension in five cases. The predisposing causes of the five patients included emotional agitations and emiction. They all did not have obvious prodromal symptoms before onset. Their presenting symtopms included distinct headache, vomiting, conscious disturbance, urine incontinence. All the patients went to coma after onset. two patients vomitted coffee-like material. One patient manifested as decerebration spasm. Two patients had speech disturbance. Crianial CT scans showed one patient with multiple cerebral hemorrhage, two patients with moderate type of right unilateral putaminalhemorrhage, one patient with left unilateral parieto-occipito-temporal subcortical hemorrhage, and one patient with severe type of right unilateral thalamus hemorrhage. These patients were diagnosed as hypertonial cerebral hemorrhage and treated with mannitol, dexamethasone, pamba. Three patients died of cerebral herniation, one patient died of stressive digestive ulcer,and one patient died of respiratory infection. On mentioning the neuroimaging characteristics of our patients, it was patient one and patient four that their hematoma were distributed as typically multifocal and subcortical demonstrated by crainial CT, and those above patients should be diagnosed highly as CAA-related hemorrhage in the clinical practice. The other three patients all had obvious mass effect and secondary injuries of the brian stem because of their hematoma, thus their prognosis were poor. According to the clinical data of our patiehts, it was suggested that the onset and clinical manifestations of patients with CAA-related hemorrhage would resemble those patients with hypertensive cerebral hemorrhage. Patients with CAA-related hemorrhage could combine with hypertension, and hypertension could aggravate CAA-related pathological changes. The typical neuroimaging of patients with CAA-related hemorrhage would shown as cortical and subcortical lobe hemorrhage, the hematoma shape was irregular and had an obvious mass effect. But CAA-related hemorrhage could not be ruled out in the setting of hemorrhage situated in plaecs such as putamen and thalamus.Part two is focused on routine neuropathological material. The cerebraltissue were fetched in 4 to 24 hours after death and were fixed in buffered 10% formalin for at least four weeks. The staining methods were Haematoxylin and Eosin, Congo red, Masson trichrome, periodic acid-Schiff(PAS) and Bodian stains. The neuropathological diagnosis were listed as the following: patient 1, left unilateral putaminal hemorrhage raptured into the lateral ventric...
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